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ChIP-Seq in DU-145 (ATCC HTB-81) Prostate Cancer Cells of FOSL1, TAZ, TEAD1, YAP

ABSTRACT: Genome-wide mapping of FOSL1, YAP, TAZ and TEAD1 binding sites in DU145 cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE196733 | GEO | 2022/02/17

REPOSITORIES: GEO

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ChIP-Seq in DU-145 (ATCC HTB-81) Prostate Cancer Cells of FOSL1, TAZ, TEAD1, YAP

Project description:ChIP-Seq in DU-145 (ATCC HTB-81) Prostate Cancer Cells of FOSL1, TAZ, TEAD1, YAP

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Project description:To explore genome-wide alteration MED1 and FOSL1 after depletion of FOSL1, we performed chromatin immunoprecipitation sequencing (ChIP-seq) of SCC1 cells to examine genome-wide recruitment of MED1 and FOSL1 following FOSL1 knockdown. Depletion of FOSL1 led to dramatically loss of the recruitment of MED1 and FOSL1 at a cohort of key oncogenes associate with tumorigenesis and metastasis.

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Genome-wide maps of YAP, TAZ and TEAD1 binding sites in human endothelial cells

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Mapping interactome networks of FOSL1 and FOSL2 in human Th17 cells

Project description:The differentiation of Th17 cells is controlled by a complex network of transcription factors (TFs), including FOS and JUN proteins of the AP-1 family. The FOS-like proteins, FOSL1 and FOSL2 have recently been reported to control Th17 responses. The molecular mechanisms dictating their roles, however, are unclear. Moreover, although the functions of AP-1 TFs are largely governed by their protein-protein interactions, these are also poorly characterized in this milieu. Using affinity purification in combination with mass-spectrometry we established the first interactomes of FOSL1 and FOSL2 in human Th17 cells. In addition to their known interactions with JUN proteins, our analysis identified several novel binding partners of FOSL factors. Gene ontology analysis revealed RNA binding was enriched as the major functionality for FOSL1 and FOSL2 associated proteins, thereby suggesting possible mechanistic links that have not been studied before. Intriguingly, 29 interactors were found to be shared between FOSL1 and FOSL2, which included crucial regulators of Th17-fate. These findings, including unique and shared interactions, were validated using parallel reaction monitoring targeted mass-spectrometry (PRM-MS), with additional measurements with other laboratory methods. Overall, this study provides key insights into interaction-based signalling mechanisms of FOSL1 and FOSL2, which potentially control Th17 cell-development and associated pathologies.

2021-11-02 | PXD025729 | Pride

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